Delayed hypersensitivity reaction after intravenous glucagon administered for a barium enema: a case report.
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INTRODUCTION: Few reports have documented allergic hypersensitivity reactions after barium gastrointestinal studies. Of these, the barium suspension, its additives or intravenous glucagon given for bowel relaxation has been implicated as possible allergens. We report a patient with delayed hypersensitivity reaction after barium enema and discuss the reasons supporting glucagon as the possible allergen. CLINICAL PICTURE: A 74-year-old Chinese woman presented with pruritic rashes, 1 day after a barium enema. Intravenous glucagon (GlucaGen, Novo Nordisk, Denmark) was administered during the barium enema. Physical examination revealed palpable purpuric rashes on the legs with erythematous papules and plaques on the arms and trunk. Skin biopsy demonstrated superficial perivascular infiltrates of lymphocytes and eosinophils, consistent with a drug eruption. TREATMENT AND OUTCOME: The rashes resolved with antihistamines and topical corticosteroids. CONCLUSION: This report highlights the potential of glucagon to cause hypersensitivity reactions. Awareness of this entity is important for the prevention and recognition of complications during barium gastrointestinal studies. (+info)
Combination of Ca2+ -activated K+ channel blockers inhibits acetylcholine-evoked nitric oxide release in rat superior mesenteric artery.
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BACKGROUND AND PURPOSE: The present study investigated whether calcium-activated K+ channels are involved in acetylcholine-evoked nitric oxide (NO) release and relaxation. EXPERIMENTAL APPROACH: Simultaneous measurements of NO concentration and relaxation were performed in rat superior mesenteric artery and endothelial cell membrane potential and intracellular calcium ([Ca2+]i) were measured. KEY RESULTS: A combination of apamin plus charybotoxin, which are, respectively, blockers of small-conductance and of intermediate- and large-conductance Ca2+ -activated K channels abolished acetylcholine (10 microM)-evoked hyperpolarization of endothelial cell membrane potential. Acetylcholine-evoked NO release was reduced by 68% in high K+ (80 mM) and by 85% in the presence of apamin plus charybdotoxin. In noradrenaline-contracted arteries, asymmetric dimethylarginine (ADMA), an inhibitor of NO synthase inhibited acetylcholine-evoked NO release and relaxation. However, only further addition of oxyhaemoglobin or apamin plus charybdotoxin eliminated the residual acetylcholine-evoked NO release and relaxation. Removal of extracellular calcium or an inhibitor of calcium influx channels, SKF96365, abolished acetylcholine-evoked increase in NO concentration and [Ca2+]i. Cyclopiazonic acid (CPA, 30 microM), an inhibitor of sarcoplasmic Ca2+ -ATPase, caused a sustained NO release in the presence, but only a transient increase in the absence, of extracellular calcium. Incubation with apamin and charybdotoxin did not change acetylcholine or CPA-induced increases in [Ca2+]i, but inhibited the sustained NO release induced by CPA. CONCLUSIONS AND IMPLICATIONS: Acetylcholine increases endothelial cell [Ca2+]i by release of stored calcium and calcium influx resulting in activation of apamin and charybdotoxin-sensitive K channels, hyperpolarization and release of NO in the rat superior mesenteric artery. (+info)
Efflux of potassium ion is an important reason of HL-60 cells apoptosis induced by tachyplesin.
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AIM: To investigate the role of intercellular potassium in tachyplesin-induced HL-60 cells apoptosis. METHODS: The concentration of intercellular potassium, cell volume and mitochondrial membrane potential were examined by flow cytometry. RESULTS: The concentration of intercellular potassium reduced in a time-dependent manner in tachyplesin-treated HL-60 cells. In addition, the loss of mitochondrial membrane potential was tightly coupled with the shrinkage of cell volume. Different caspase inhibitors protected against DNA degradation but did not prevent the loss of HL-60 cell viability induced by tachyplesin. Ba2+, which was a kind of blocker of volume-regulatory K+ channels, increased the viability of tachyplesin-treated HL-60 cells and maintained mitochondrial membrane potential and cell volume. CONCLUSION: Efflux of K+ was an important reason for apoptosis in tachyplesin-treated HL-60 cells. Efflux of K+ affected the viability of tachyplesin-treated HL-60 cells independent of the process of caspase activation. (+info)
Pharmacology of the Ca2(+)-dependent K+ channel in corn protoplasts.
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We investigated the sensitivity of the Ca2(+)-dependent K+ current, IK(Ca), present in corn protoplasts, to different K+ channel blockers. IK(Ca) was inhibited by external Cs+ (10 mM), Ba2+ (10 mM), and quinine (0.5 mM): reagents which block many types of outward-rectifying K+ channels. In contrast 4-aminopyridine (5 mM), an inhibitor of delayed rectifier or inactivating K+ currents, had no effect. Neither of the peptide toxins, apamin or charybdotoxin, specific for Ca2(+)-dependent K+ channels in animal cells, inhibited currents when used in the nanomolar concentration range. However, higher levels of charybdotoxin (10 microM) caused marked reduction of IK(Ca). (+info)
Whole-cell and single channel K+ and Cl- currents in epithelial cells of frog skin.
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Whole-cell and single channel currents were studied in cells from frog (R. pipiens and R. catesbiana) skin epithelium, isolated by collagenase and trypsin treatment, and kept in primary cultures up to three days. Whole-cell currents did not exhibit any significant time-dependent kinetics under any ionic conditions used. With an external K gluconate Ringer solution the currents showed slight inward rectification with a reversal potential near zero and an average conductance of 5 nS at reversal. Ionic substitution of the external medium showed that most of the cell conductance was due to K and that very little, if any, Na conductance was present. This confirmed that most cells originate from inner epithelial layers and contain membranes with basolateral properties. At voltages more positive than 20 mV outward currents were larger with K in the medium than with Na or N-methyl-D-glucamine. Such behavior is indicative of a multi-ion transport mechanism. Whole-cell K current was inhibited by external Ba and quinidine. Blockade by Ba was strongly voltage dependent, while that by quinidine was not. In the presence of high external Cl, a component of outward current that was inhibited by the anion channel blocker diphenylamine-2-carboxylate (DPC) appeared in 70% of the cells. This component was strongly outwardly rectifying and reversed at a potential expected for a Cl current. At the single channel level the event most frequently observed in the cell-attached configuration was a K channel with the following characteristics: inward-rectifying I-V relation with a conductance (with 112.5 mM K in the pipette) of 44 pS at the reversal potential, one open and at least two closed states, and open probability that increased with depolarization. Quinidine blocked by binding in the open state and decreasing mean open time. Several observations suggest that this channel is responsible for most of the whole-cell current observed in high external K, and for the K conductance of the basolateral membrane of the intact epithelium. On a few occasions a Cl channel was observed that activated upon excision and brief strong depolarization. The I-V relation exhibited strong outward rectification with a single channel conductance of 48 pS at 0 mV in symmetrical 112 mM Cl solutions. Kinetic analysis showed the presence of two open and at least two closed states. Open time constants and open probability increased markedly with depolarization.(ABSTRACT TRUNCATED AT 400 WORDS) (+info)
Sevoflurane breakdown produces flammable concentrations of hydrogen.
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BACKGROUND: Fires, explosions, and extreme heat production may occur when sevoflurane reacts with desiccated barium hydroxide lime. The identity of the flammable gas has not previously been published, although carbon monoxide, methanol, formaldehyde, and methyl formate have been identified in low quantities. METHODS: The authors reacted sevoflurane with excess desiccated barium hydroxide lime or soda lime at 55 degrees, 100 degrees, 200 degrees, 300 degrees, and 400 degrees C. Formaldehyde, methanol, sodium formate, and hexafluoroisopropanol were reacted with barium hydroxide lime at 300 degrees or 400 degrees C. The authors measured hydrogen production by gas chromatography with a thermal conductivity detector and calculated the molar yield of hydrogen produced. RESULTS: Up to 3 moles of hydrogen were produced per mole of sevoflurane degraded. Each mole of formaldehyde produced up to 2 moles of hydrogen at 400 degrees C. Formate and hexafluoroisopropanol produced up to 1 mole of hydrogen each at 400 degrees C. More than 2 moles of hydrogen were produced by methanol at 400 degrees C. Soda lime and barium hydroxide lime produced similar amounts of hydrogen from sevoflurane above 200 degrees C, but barium hydroxide lime produced more than soda lime at lower temperatures. The temperature above which large amounts of hydrogen were produced seemed to be 300 degrees C. CONCLUSIONS: Up to 3 moles of hydrogen are produced by the chemical reaction of sevoflurane with heated, desiccated absorbent. The high yield, ease of ignition, and low tissue solubility of hydrogen make it the most likely fuel in anesthesia machine fires due to the reaction of sevoflurane with desiccated absorbent. (+info)
Roles of potassium and chloride ions in cAMP-mediated amylase exocytosis from rat parotid acini.
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The roles of potassium and chloride ions in cAMP-mediated amylase exocytosis were studied using intact and saponin-permeabilized parotid acini. Cyclic AMP-evoked amylase release from saponin-permeabilized parotid acini decreased markedly when KCl in the incubation medium was isoosmotically replaced by K-glutamate, NaCl, Na-isothionate, or mannitol. Quinidine and barium, K+ channel blockers, clearly inhibited amylase release from the permeabilized acini, but not from intact ones. The chloride channel blocker DPC (diphenylamine-2-carboxylate) also inhibited amylase release, while DIDS (4,4'-diisothiocyanostilben-2,2'-disulfonate) or bumetanide had little effect, if any, on the exocytosis. Hyperosmolarity with mannitol markedly reduced amylase release from permeabilized acini. These results suggest that potassium and chloride ions play important roles in cAMP-mediated amylase exocytosis, and that these ions act on secretory granules inside the acinar cells. (+info)
G protein-coupled inwardly rectifying potassium channels in dorsal root ganglion neurons.
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AIM: G protein-coupled inwardly rectifying potassium channels (GIRK) are important for neuronal signaling and membrane excitability. In the present study, we intend to find whether GIRK channels express functionally in adult rat dorsal root ganglion (DRG) neurons. METHODS: We used RT-PCR to detect mRNA for 4 subunits of GIRK in the adult DRG. The whole-cell patch clamp recording was used to confirm GIRK channels functionally expressed. RESULTS: The mRNA for the 4 subunits of GIRK were detected in the adult DRG. GTPgammaS enhanced inwardly rectifying potassium (K+) currents of the DRG neurons, while Ba2+ inhibited such currents. Furthermore, the GIRK channels were shown to be coupled to the GABA(B) receptor, a member of the G protein-coupled receptor family, as baclofen increased the inwardly rectifying K+ currents. CONCLUSION: GIRK channels are expressed and functionally coupled with GABA(B) receptors in adult rat DRG neurons. (+info)